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246 related items for PubMed ID: 19243453

  • 1. Neurodevelopmental delay in the Cln3Deltaex7/8 mouse model for Batten disease.
    Osório NS, Sampaio-Marques B, Chan CH, Oliveira P, Pearce DA, Sousa N, Rodrigues F.
    Genes Brain Behav; 2009 Apr; 8(3):337-45. PubMed ID: 19243453
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  • 3. Finding the most appropriate mouse model of juvenile CLN3 (Batten) disease for therapeutic studies: the importance of genetic background and gender.
    Kovács AD, Pearce DA.
    Dis Model Mech; 2015 Apr; 8(4):351-61. PubMed ID: 26035843
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  • 4. Altered sensitivity of cerebellar granule cells to glutamate receptor overactivation in the Cln3(Δex7/8)-knock-in mouse model of juvenile neuronal ceroid lipofuscinosis.
    Finn R, Kovács AD, Pearce DA.
    Neurochem Int; 2011 May; 58(6):648-55. PubMed ID: 21315126
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  • 10. Partial correction of the CNS lysosomal storage defect in a mouse model of juvenile neuronal ceroid lipofuscinosis by neonatal CNS administration of an adeno-associated virus serotype rh.10 vector expressing the human CLN3 gene.
    Sondhi D, Scott EC, Chen A, Hackett NR, Wong AM, Kubiak A, Nelvagal HR, Pearse Y, Cotman SL, Cooper JD, Crystal RG.
    Hum Gene Ther; 2014 Mar; 25(3):223-39. PubMed ID: 24372003
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  • 11. Retinal function in aging homozygous Cln3 (Δex7/8) knock-in mice.
    Volz C, Mirza M, Langmann T, Jägle H.
    Adv Exp Med Biol; 2014 Mar; 801():495-501. PubMed ID: 24664736
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  • 12. Developmental impairments of select neurotransmitter systems in brains of Cln3(Deltaex7/8) knock-in mice, an animal model of juvenile neuronal ceroid lipofuscinosis.
    Herrmann P, Druckrey-Fiskaaen C, Kouznetsova E, Heinitz K, Bigl M, Cotman SL, Schliebs R.
    J Neurosci Res; 2008 Jun; 86(8):1857-70. PubMed ID: 18265413
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  • 13. Further Characterization of the Predominant Inner Retinal Degeneration of Aging Cln3 Δex7/8 Knock-In Mice.
    Volz C, Mirza M, Langmann T, Jägle H.
    Adv Exp Med Biol; 2018 Jun; 1074():403-411. PubMed ID: 29721970
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  • 14. Microglia in juvenile neuronal ceroid lipofuscinosis are primed toward a pro-inflammatory phenotype.
    Xiong J, Kielian T.
    J Neurochem; 2013 Oct; 127(2):245-58. PubMed ID: 23919525
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  • 15. Astrocytes in juvenile neuronal ceroid lipofuscinosis (CLN3) display metabolic and calcium signaling abnormalities.
    Bosch ME, Kielian T.
    J Neurochem; 2019 Mar; 148(5):612-624. PubMed ID: 29964296
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  • 16. A knock-in reporter mouse model for Batten disease reveals predominant expression of Cln3 in visual, limbic and subcortical motor structures.
    Ding SL, Tecedor L, Stein CS, Davidson BL.
    Neurobiol Dis; 2011 Feb; 41(2):237-48. PubMed ID: 20875858
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  • 17. Immunomodulation with minocycline rescues retinal degeneration in juvenile neuronal ceroid lipofuscinosis mice highly susceptible to light damage.
    Dannhausen K, Möhle C, Langmann T.
    Dis Model Mech; 2018 Sep 05; 11(9):. PubMed ID: 30042155
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  • 18. Loss of CLN3, the gene mutated in juvenile neuronal ceroid lipofuscinosis, leads to metabolic impairment and autophagy induction in retinal pigment epithelium.
    Zhong Y, Mohan K, Liu J, Al-Attar A, Lin P, Flight RM, Sun Q, Warmoes MO, Deshpande RR, Liu H, Jung KS, Mitov MI, Lin N, Butterfield DA, Lu S, Liu J, Moseley HNB, Fan TWM, Kleinman ME, Wang QJ.
    Biochim Biophys Acta Mol Basis Dis; 2020 Oct 01; 1866(10):165883. PubMed ID: 32592935
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  • 19. Cln3-mutations underlying juvenile neuronal ceroid lipofuscinosis cause significantly reduced levels of Palmitoyl-protein thioesterases-1 (Ppt1)-protein and Ppt1-enzyme activity in the lysosome.
    Appu AP, Bagh MB, Sadhukhan T, Mondal A, Casey S, Mukherjee AB.
    J Inherit Metab Dis; 2019 Sep 01; 42(5):944-954. PubMed ID: 31025705
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  • 20. Caspase 1 activity influences juvenile Batten disease (CLN3) pathogenesis.
    Burkovetskaya M, Bosch ME, Karpuk N, Fallet R, Kielian T.
    J Neurochem; 2019 Mar 01; 148(5):652-668. PubMed ID: 29873075
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